Associates with IL12B to form the pro-inflammatory cytokine IL-23 that plays different roles in innate and adaptive immunity. Released by antigen-presenting cells such as dendritic cells or macrophages, binds to a heterodimeric receptor complex composed of IL12RB1 and IL23R to activate JAK2 and TYK2 which then phosphorylate the receptor to form a docking site leading to the phosphorylation of STAT3 and STAT4. This process leads to activation of several pathways including p38 MAPK or NF-kappa-B and promotes the production of pro-inflammatory cytokines such as interleukin-17A/IL17A. In turn, participates in the early and effective intracellular bacterial clearance. Promotes the expansion and survival of T-helper 17 cells, a CD4-positive helper T-cell subset that produces IL-17, as well as other IL-17-producing cells.
IL-23 , which is mainly secreted by antigen-presenting cells , is a member of the IL-12 family , which includes IL-12 , IL-27 , and IL-35. IL-23 is a heterodimeric cytokine , comprised of a unique p19 subunit and p4 subunit , the latter of which is shared with IL-12. The receptor for IL-23 consists of IL-23R and IL-12Rβ1 , the latter of which is also characteristic of IL-12. IL-23 is essential for Th17 differentiation , expansion , and survival by binding to its receptor , thereby activating the signaling pathway. Many studies revealed that the IL-23/Th17 pathway is implicated in the pathophysiology of various autoimmune diseases , such as autoimmune arthritis , primary biliary cirrhosis , and inflammatory bowel disease.
Interleukin 23 receptor (IL23R) is a type I cytokine receptor for IL23. IL23 receptor complex is comprised of two subunits; the IL12Rβ1 subunit; which is shared with several cytokines; and a subunit that is unique to IL-23. IL23; after binding to IL23R; activates memory T cells and mediates pro-inflammatory activities in part by the production of IL17 through activation of TH17 lymphocytes. IL23R is expressed on T cells; NK cells; dendritic cells; and macrophages. In fact; polymorphisms of the IL23R gene were reported to be associated with susceptibility to inflammatory diseases and autoimmune diseases such as psoriasis; multiple sclerosis; Graves's ophtalmopathy and inflammatory bowel diseases. The IL23R is known to be critically involved in the carcinogenesis of different malignant tumor.
Multifunctional cytokine mainly produced by T-cells that plays a regulatory role in immune response, tissue homeostasis, host defense, and oncogenesis. Possesses antiviral functions and induces the type I intereferon response during influenza infection. Signals through two receptor complexes IL20RA/IL20RB or IL20RB/IL22RA1. In turn, stimulates the JAK1-STAT3 and MAPK pathways and promotes the secretion of pro-inflammatory mediators including IL8 and MMP1. Intracellularly, maintains endoplasmic reticulum homeostasis by restricting the eIF2alpha-CHOP pathway-mediated stress signal. In addition, acts as a quality control mechanism for the ubiquitin proteasome system by alerting the cell to proteasome dysfunction through activation of PKR/EIF2AK2.
Interleukin-25(IL-25) is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. IL-25 is a member of the IL-17 family of cytokines. However, unlike the other members of this family, IL-25 promotes T helper(Th) 2 responses. IL-25 also regulates the development of autoimmune inflammation mediated by IL-17–producing T cells. IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin(TSLP) –activated dendritic cells(DCs), homeostatic cytokines, or T cell receptor for antigen triggering. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. A plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells had been provided.
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